Positron emission tomographic scanning demonstrates a presynaptic dopaminergic lesion in Lytico-Bodig. The amyotrophic lateral sclerosis-parkinsonism-dementia complex of Guam
B. J. Snow, R. F. Peppard, M. Guttman, J. Okada, W. R. Martin, J. Steele, A. Eisen, G. Carr, B. Schoenberg and D. Calne
Belzberg Laboratory of Clinical Neurosciences, Division of Neurology, University of British Columbia, Vancouver.
We performed positron emission tomography using 18F-6-fluorodopa on four
Guamanians with an amyotrophic lateral sclerosis syndrome, eight Guamanians
with parkinsonism, and seven clinically normal Guamanians; the results were
compared with those of nine Vancouver control subjects. The Guamanian
subjects had all been exposed to similar Chamorro lifestyles. The scans
were analyzed using a graphic method that calculates a constant for whole
striatal 18F-6-fluorodopa uptake. The parkinsonian subjects all had
significantly reduced striatal 18F-6-fluorodopa uptake. The group with
amyotrophic lateral sclerosis had significantly reduced uptake that was
intermediate between that of the control group and the parkinsonian group.
Two Guamanian normal subjects had reduced striatal 18F-6-fluorodopa uptake.
The nigrostriatal dopaminergic lesion in Guamanian parkinsonism is similar
to that found in idiopathic parkinsonism. The nigrostriatal lesions in the
subjects with amyotrophic lateral sclerosis and the Guamanian normal
subjects are examples of subclinical neuronal damage demonstrable in living
subjects with positron emission tomography.
